Antibiotic Classification and General Information

Protein synthesis inhibitors

Major groups: aminoglycosides, tetracyclines, macrolides

General mechanism of action: Protein synthesis inhibiting antibiotics primarily target the bacterial ribosome (70S) which is made up of a small, 30S subunit and a large, 50S subunit. A ribosome is an essential, complex molecule made up of proteins and RNA and is responsible for synthesizing proteins. Aminoglycosides, macrolides, and other protein synthesis inhibitors target and prevent specific stages of protein synthesis at specific locations on 70S ribosomes. Bacterial death occurs because the cell cannot make proteins required for essential cellular processes.

Effects on humans – Humans, and other eukaryotic cells synthesize proteins using a 80S (not 70S) ribosome which is not targeted by these inhibitors. (other side effects are possible)

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Protein Synthesis Inhibitors
 
 
 
30S Subunit
50S Subunit

EF-G

 
 
 
 
 

Aminoglycosides
(initiation inhibitors)

Tetracycline antibiotics
(rRNA binding)

Peptidyl 
transferase

MLS 
(transpeptidation
/tranaslocation)

Steroid Antibacterials

 
 
 
 
 
 
 
 
 

-mycin
(Streptomyces)

-micin 
(Micromonospora)

Tetracyclines

Glycylcyclines

Amphenicols

Pleuromutilins

Macrolides

Lincosamides

 
 
 
 
 
 
 
 
Protein Synthesis Inhibitors

Nucleic acid synthesis inhibitors

Major groups: Antifolates, topoisomerase inhibitors (floroquinolones)

General mechanism of action: These antibiotics target different stages and pathways of nucleic acid (DNA, RNA…) synthesis. In summary, antifolates (includes sulfonamides) inhibit enzymes involved in folate/folic acid (vitamin B9) synthesis. Folate is an essential ingredient for the synthesis of pyrimidine and purines, two molecules found in nucleotides, the building blocks of DNA and other nucleic acids. Topoisomerase inhibitors prevent DNA replication by inhibiting topoisomerase activity. Toposiomerases are enzymes that relieve DNA supercoil stress during DNA replication. By inhibiting topoisomerase activity, DNA replication is greatly hindered and cell division rate is diminished.

Effects on humans – Humans acquire folate from dietary sources, they do not have a synthesis pathway for folate and are not affected by antifolates in the same way bacteria are. Topoisomerases can be found in human cells; however the molecular makeup of human topoisomerases differs from those found in bacteria. (other side effects are possible)

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Nucleic Acid Inhibitors
 
 
 
 
Antifolates
Topoisomerase Inhibitors and quinolones
 
 
 
 

DHFR inhibitor

Sulfonamides
(DHPS inhibitor)

1st generation

Fluoroquinolones

 
 
 
 
 
 
 
 
 

Short-acting

Intermediate

Long-acting

2nd generation

3rd generation

4th generation

Related(DG)

 
 
 
 
 
 
 
Anaerobic DNA
inhibitors
RNA synthesis
 
 
 

Nitro-imidazole derivatives

Nitrofuran derivatives

Rifamycins/RNA polymerase

 
 
 
Nucleic Acid synthesis

Cell wall synthesis inhibitors

Major groups: Beta-lactams (cephalosporins, penicillins)

General mechanism of action: As the name implies, this group of antibiotics inhibits certain stages in bacterial cell wall synthesis. A major structural component in the bacterial cell wall (more so in Gram-positive bacteria) is an essential polymer called peptidoglycan. Beta-lactam antibiotics bind to PBPs or penicillin binding proteins which are involved in the final stages of peptidoglycan synthesis. By inhibiting PBP function, peptidoglycan cannot be properly synthesized and the cell lyses.

Effects on humans – Human cells do not use nor synthesize peptidoglycan and are therefore not susceptible to beta-lactam antibiotics. (other side effects are possible)

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Antibacterials:cell envelope antibiotics
 
 
 
 

Intracellular

Glycopeptide

 
 
Cell wall synthesis